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Is a condition that results from failure in the negative feedback mechanism that regulates

inhibition and secretion of ADH. It produces excess ADH, resulting hypothermia and
hypoosmolality of serum. The kidneys respond by reabsorbing water in the tubules and excreting
sodium; thus the patient becomes severely water intoxicated. SIADH is most commonly caused
by ectopic production of ADH by malignant tumors. It can be result of CNS disorders, such as
Guillain-Barre syndrome, meningitis, brain tumors, and head trauma. Pulmonary-related
conditions, such as pneumonia, and positive pressure ventilation can cause SIADH.
Pharmacologic agents such as general anesthetics, thiazine diuretics, oral hypoglycemics,
chemotherapeutic agents, and analgesics are also associated with SIADH release.

Signs And Symptoms

Vital signs

 BP: Increased or may be normal


 HR: tachycardia
 Temperature: decreased or may be normal

Neurologic

 Alert to unresponsiveness
 Seizures

Cardiovascular

 Bounding pulses

Pulmonary

 Crackles may be present

Gastrointestinal

 Cramps
 Decreased bowel sounds
 Vomiting

Muscoloskeletal

 Weakness
 Cramps
 Absent deep tension reflexes

Acute Care Patient Management


Nursing Dianosis: Excess fluid volume related to excessive amount of antidiuretic hormone
secretion.

Outcome Criteria

 Intake approximates output


 Serum potassium 3.5 to 5 mEq/L
 Serum sodium 135 to 145 mEq/L
 Serum chloride 95 to 105 mEq/L
 Serum osmolality 275 to 295 mOsm/kg
 Urine specific gravity 1.003 to 1.035
 CVP 2 to 6 mm Hg

Patient Monitoring

1. Monitor pulmonary artery pressures and central venous pressure hourly (if available) or
more frequently to evaluate the patient’s response to treatment. Both parameters reflect
the capacity of the vascular system to accept volume and can be used to monitor fluid
volume status.
2. Monitor hourly intake and output, and determine fluid balance every 8 hours. Compare
serial weights and note rapid (0.5-1 kg/day) changes in weight, suggesting fluid
imbalance.
3. Continuously monitor ECG for dysrhythmias resulting from electrolyte imbalance.

Patient Assessment

1. Obtain VS every hour or more frequently until the patient’s condition is stable.
2. Evaluate hydration status every 4 hours. Note skin turgor on inner thigh or forehead,
condition or buccal membranes, development of edema or crackles, and complaints of
thirst.
3. Assess for pressure ulcer development secondary to edematous state.

Diagnostic Assessment

1. Review serum sodium and potassium, serum osmolality, urine specific gravity, and urine
osmolality to evaluate the patient’s response to therapy.

Patient Management

1. Restrict fluid as ordered, generally <500 mL/day in severe cases and 800 to 1000 mL/day
in moderate cases.
2. Administer potassium supplements as ordered, assess renal function and ensure adequate
urine output before administering potassium.
3. As adjuncts to water restriction, demeclocycline may be ordered to inhibit the renal
response to ADH in patients with lung malignancies.
4. Avoid hypotonic enemas to treat constipation because water intoxication can be
potentiated.
5. Institute pressure ulcer prevention strategies.

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